Recent studies have indicated that fast arm movements in humans are started and stopped by the preprogrammed timing and amplitude of agonist-antagonist EMG activity. The hypothesis to be tested in the present proposal is that the cerebellum normally contributes to this preprogramming. Consequently during cerebellar dysfunction movements are no longer accurately preprogrammed and thus are started abnormally, and are stopped inappropriately by stretch reflexes (spinal and transcortical). The long term objectives are to determine the role of the cerebellum in the preprogramming of normal movements and to determine the mechanisms underlying cerebellar ataxia. The specific aims are: 1) To determine the relationship between agonists and antagonists in normal fast elbow movements made by monkeys, to determine how it is changed in dysmetria and thereby to discover what causes dysmetria at the muscle level, 2) To determine the effect of altering proprioceptive and visual feedback on dysmetria, 3) To determine the changes that occur in agonist and antagonist related motor cortex neurons during cerebellar dysfunction. Temporary cerebellar dysfunction will be produced by cooling through probes implanted lateral and medial to dentate. Such cooling produces an animal model which displays all the characteristics of classic cerebellar ataxia described by neurologists but has the advantage of being reversible, the motor disorder lasting only as long as the cooling is applied. The technique will enable a comparison to be made of the normal activity of motor units and single neurons in motor cortex and the changed activity during cerebellar dysfunction.